A role for the nicotinic alpha-bungarotoxin receptor in neurite outgrowth in PC12 cells

Neuroscience. 1993 Sep;56(2):441-51. doi: 10.1016/0306-4522(93)90344-f.


The addition of nicotine decreased neuritic outgrowth in PC12 cells in culture. This effect occurs as early as one day after addition of nicotine to the culture medium in a concentration-dependent manner. The nicotine-induced decline in neurite outgrowth was prevented by d-tubocurarine (10(-4) M) indicating that the effect was mediated through a nicotinic receptor. alpha-Bungarotoxin (10(-8) M) was also able to inhibit the nicotine-induced decrease in process formation in a dose-dependent manner. The concentrations of alpha-bungarotoxin required to affect process outgrowth correlated with those required to inhibit radiolabelled alpha-bungarotoxin binding. alpha-Bungarotoxin had no effect on [3H]noradrenaline release, a functional response mediated through the alpha-bungarotoxin-insensitive neuronal nicotinic acetylcholine receptor, suggesting that alpha-bungarotoxin specifically interacts with the neuronal alpha-bungarotoxin receptor. The present results suggest a functional role for the neuronal nicotinic alpha-bungarotoxin receptor in neurite outgrowth.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bungarotoxins / pharmacology*
  • Nerve Growth Factors / pharmacology
  • Neurites / drug effects
  • Neurites / physiology*
  • Nicotine / pharmacology
  • Norepinephrine / metabolism
  • PC12 Cells / drug effects
  • PC12 Cells / physiology*
  • PC12 Cells / ultrastructure
  • Rats
  • Receptors, Nicotinic / physiology*
  • Tubocurarine / pharmacology
  • alpha7 Nicotinic Acetylcholine Receptor


  • Bungarotoxins
  • Chrna7 protein, rat
  • Nerve Growth Factors
  • Receptors, Nicotinic
  • alpha7 Nicotinic Acetylcholine Receptor
  • Nicotine
  • Tubocurarine
  • Norepinephrine